Cystic Fibroses (CF) is a recessive genetic disease caused by mutations in a membrane-associated protein, which promotes transcellular movement of chloride ions in airway epithelia and other tissues. In the lungs, defective function of the membrane-associated protein results in abnormally thick secretions in the lower airways which plug small bronchioles and provide an environment for chronic endobronchincal bacterial infection. Despite recruitment of vast numbers of neutrophils, bacterial clearance is ineffective, and the airways of the lungs are damaged by free radical species and prostheses released by the neutrophils. In addition, as the recruited neutrophils decompose in the airway, the DNA from their nuclei markedly increase the viscosity of the lower airway secretions, leading to further airway blockage and infection. The end result of this above-identified cycle is destruction of bronchial airway structure and progressive loss of lung function in the CF patient. Despite significant improvements in clinical management, respiratory failure and related pulmonary complications account for over ninety percent of CF mortality.
Since pulmonary disease is the primary cause of morbidity and mortality in CF, considerable effort has been directed to increase the mobilization of the abnormally thick airway secretions through various forms of chest physiotherapy. In the normal respiratory system, there are three primary mucus transport mechanisms. First, as is predominate in the smaller airways of the lungs, is a conveyor-like effect of a coordinated beating of airway epthocilia. In the larger airways, the second method of mucus transport is the high velocity airflow associated with coughing. Coughing tends to sheer mucus off airway surfaces and propels it towards the pharynx. The third mechanism of transporting mucus through the lungs is termed cephalad airflow bias of tidal breathing. Cephalad airflow bias results from greater expiratory versus inspiratory airflow due to compression of the intrathorasic airways during expiration. However, the abnormal composition and increased amount of tracheal bronchial secretions in the airways of a CF patient impede all of these natural mechanisms of mucus clearance.
For this reason, several forms of chest physiotherapy have been developed. These methods of chest physiotherapy are intended to assist in pulmonary mucus clearance and are presently widely used for CF patients. The mechanism underlying all modes of chest physiotherapy currently in use is vibration of the airway surfaces, either through external chest compression or by oscillatory airflow, to promote increased cephalad-induced and/or cough-induced mobilization of airway secretions.
Currently, the most common form of chest physiotherapy is manual chest physiotherapy. In manual chest physiotherapy a trained caregiver strikes the patient's chest with cupped hands. This striking motion is usually complimented with postural drainage, a systematic form of directing mucus from the peripheral to the central airways through a series of gravity-assisted patient positions and therapist simulation. Each physiotherapy session is coupled with a period of huffing and coughing to remove sputum. While this method of therapy is somewhat effective, manual chest physiotherapy is labor intensive because it must be performed by a therapist or trained caregiver. The efficacy of manual chest therapy depends on the skill and diligence of the therapist. For this reason, manual chest physiotherapy may be expensive and/or time consuming for the therapist and patient. Additionally, the striking of the chest may cause discomfort to the patient or damage to a more fragile patient's ribcage.
Various mechanical devices have been developed in an effort to standardize and increase the efficiency of chest physiotherapy. Among the most widely employed forms of mechanical chest physiotherapy are various hand-held compressors which deliver external chest vibration, high frequency chest compression administered through an inflatable jacket, and devices such as a FLUTTER™ device which delivers internal airway stimulation from pulsating airflow via the mouth.
The high frequency chest compression (HFCC) method of chest physiotherapy is very commonly employed today. HFCC is administered via a product called the VEST™. In clinical studies with CF patients, use of the VEST™ has been shown to be a practical, automated method of chest physiotherapy, and is an improvement over manual therapy to the extent that it allows for increased patient independence. HFCC, via oscillating chest compression, stimulates cough with its associated mucus shearing airflow spikes, and the compression of the thorax during expiration results in increased expiratory airflow. It is hypothesized also that HFCC at certain frequencies promotes a longer ciliary brush stroke, thereby enhancing mucus transport.
The VEST™ device consists of an inflatable vest structure which is strapped onto the patient's torso. The inflatable vest structure is attached by supply tubes to an air compressor. The air compressor is powered such that it can force air into the vest worn by the patient at set frequencies and amplitudes. In this way, the vest that the patient wears is inflated to compress the patient's chest at set frequencies and amplitudes.
With the present mechanical devices such as the VEST™, the oscillating pressure administered to the chest wall is not transmitted equally across the chest to the underlying lung. Increased mucus transport only occurs in those portions of the lungs directly covered by the isolating pressure vest. In particular, with the VEST™ device the lungs are excited from the sides but not from the top or bottom. The pressure administered by the VEST™ device is not uniform. The pressures applied to the patient's chest varies greatly. Additionally, the frequency at which the vest operates is not fine-tuned such as to optimize airway stimulation with the least amount of applied external energy. Generally, in clinical use of the VEST™, patients adjust the frequency and amplitude of the applied chest wall stimulation to what they believe provides the best results or to the maximum they can tolerate.
In addition to the above-referenced shortcomings of the prior art chest physiotherapy regimens, the current methods of chest physiotherapy are generally quite uncomfortable. Most of the current methods of chest physiotherapy require a force to be exerted on the external chest cavity of the patient. This is disadvantageous to all patients, but particularly to those who are more prone to rib or chest injury due to the impact, such as frail or elderly patients and very young patients.
Therefore, it would be desirable to have a method and apparatus for chest physiotherapy that does not involve a trained caregiver or physiotherapist, such as to minimize cost, increase the patient's independence, and also involves a marginal, if any amount of impact to the CF patient's chest. It is also desirable to have a method and apparatus for chest physiotherapy that does not cause discomfort to the patient, applies more uniform stimulation to the lungs and excites the entire lung. The invention described in detail below meets the limitations of the prior art.